Reticulon 4

Reticulon 4
Reticulon 4

PDB rendering based on 2g31.
Symbols RTN4; ASY; NI220/250; NOGO; NOGO-A; NOGOC; NSP; NSP-CL; Nbla00271; Nbla10545; Nogo-B; Nogo-C; RTN-X; RTN4-A; RTN4-B1; RTN4-B2; RTN4-C
External IDs OMIM604475 MGI1915835 HomoloGene10743 GeneCards: RTN4 Gene
RNA expression pattern
PBB GE RTN4 211509 s at tn.png
PBB GE RTN4 210968 s at tn.png
PBB GE RTN4 214629 x at tn.png
More reference expression data
Species Human Mouse
Entrez 57142 68585
Ensembl ENSG00000115310 ENSMUSG00000020458
UniProt Q9NQC3 Q99P72
RefSeq (mRNA) NM_007008.2 NM_024226
RefSeq (protein) NP_008939.1 NP_077188
Location (UCSC) Chr 2:
55.2 – 55.34 Mb
Chr 11:
29.59 – 29.64 Mb
PubMed search [1] [2]

Reticulon-4, also known as Neurite outgrowth inhibitor or Nogo, is a protein that in humans is encoded by the RTN4 gene[1][2][3] that has been identified as an inhibitor of neurite outgrowth specific to the central nervous system.

This gene belongs to the family of reticulon-encoding genes. Reticulons are associated with the endoplasmic reticulum, and are involved in neuroendocrine secretion or in membrane trafficking in neuroendocrine cells. The product of this gene is a potent neurite outgrowth inhibitor that may also help block the regeneration of the central nervous system in higher vertebrates. Alternatively spliced transcript variants derived both from differential splicing and differential promoter usage and encoding different isoforms have been identified.[3] There are three isoforms: Nogo A, B and C. Nogo-A has two known inhibitory domains including amino-Nogo, at the N-terminus and Nogo-66, which makes up the molecules extracellular loop. Both amino-Nogo and Nogo-66 are involved in inhibitory responses, where amino-Nogo is a strong inhibitor of neurite outgrowth, and Nogo-66 is involved in growth cone destruction.[4]

Research suggests that blocking Nogo-A during neuronal damage (from diseases such as Multiple Sclerosis) will help to protect or restore the damaged neurons.[4] The investigation into the mechanisms of this protein presents a great potential for the treatment of auto-immune mediated demyelinating diseases and spinal cord injury regeneration. It has also been found to be a key player in the process whereby physical exercise enhances learning and memory processes in the brain.[5]



Reticulon 4 has been shown to interact with WWP1,[6] BCL2-like 1[7] and Bcl-2.[7]

See also


  1. ^ GrandPre T, Nakamura F, Vartanian T, Strittmatter SM (Feb 2000). "Identification of the Nogo inhibitor of axon regeneration as a Reticulon protein". Nature 403 (6768): 439–44. doi:10.1038/35000226. PMID 10667797. 
  2. ^ Yang J, Yu L, Bi AD, Zhao SY (Jun 2000). "Assignment of the human reticulon 4 gene (RTN4) to chromosome 2p14-->2p13 by radiation hybrid mapping". Cytogenet Cell Genet 88 (1-2): 101–2. doi:10.1159/000015499. PMID 10773680. 
  3. ^ a b "Entrez Gene: RTN4 reticulon 4". 
  4. ^ a b Karnezis et al.; Mandemakers, W; McQualter, JL; Zheng, B; Ho, PP; Jordan, KA; Murray, BM; Barres, B et al. (2004). "The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination.". Nature Neuroscience 7 (7): 736–744.. doi:10.1038/nn1261. PMID 15184901. 
  5. ^ Stopping a receptor called 'nogo' boosts the synapses
  6. ^ Qin, Haina; Pu Helen X, Li Minfen, Ahmed Sohail, Song Jianxing (Dec. 2008). "Identification and structural mechanism for a novel interaction between a ubiquitin ligase WWP1 and Nogo-A, a key inhibitor for central nervous system regeneration". Biochemistry (United States) 47 (51): 13647–58. doi:10.1021/bi8017976. PMID 19035836. 
  7. ^ a b Tagami, S; Eguchi Y, Kinoshita M, Takeda M, Tsujimoto Y (Nov. 2000). "A novel protein, RTN-XS, interacts with both Bcl-XL and Bcl-2 on endoplasmic reticulum and reduces their anti-apoptotic activity". Oncogene (England) 19 (50): 5736–46. doi:10.1038/sj.onc.1203948. ISSN 0950-9232. PMID 11126360. 

Further reading

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